Inhibitor κBα protein therapy alleviates severe pneumonia through inhibition of nuclear factor κB.

To investigate the effect of inhibitor κBα (IκBα) on severe pneumonia and explain the mechanisms of nuclear factor κB (NF-κB), the activation of NF-κB was induced in Sprague-Dawley (SD) rats infected with (). The rats were then treated with differing concentrations of IκBα protein. A histological analysis was performed to compare the lung structure prior to and following treatment, and an immunohistochemistry assay was used to detect NF-κB activity. In addition, the expression of certain inflammatory factors was detected using a protein chip assay. The severe pneumonia rat model was successfully produced and in model rats, NF-κB was activated by . Following treatment with IκBα, the activity of NF-κB was inhibited and pneumonia symptoms in model rats were alleviated. Furthermore, the expression of a number of inflammatory factors including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), interferon γ (IFN-γ) and monocyte chemoattractant protein-1 (MCP-1) were also inhibited. The current study demonstrates that NF-κB inhibition with IκBα protein therapy prevents the development of pneumonia in a rat model. The therapeutic effect is indicated by the responses of proinflammatory factors, including TNF-α, IL-6, IFN-γ and MCP-1.